Fat‑cell memory drives weight regain

A mouse study finds brief exposure to the inflammatory cytokine TGF‑β1 remodels adipose chromatin to expose the asprosin precursor gene, raising persistent asprosin production and appetite; genetically removing asprosin or its receptor blocks the effect, and maternal TGF‑β1 exposure may transmit elevated asprosin to offspring. If replicated in humans, this identifies an epigenetic 'memory' mechanism in fat cells that helps explain rapid weight relapse after stopping drugs like GLP‑1s. — This suggests obesity treatments must address durable adipose‑cell programming (not just energy balance) and points to asprosin blockade as a candidate strategy to prevent post‑treatment rebound and intergenerational risk.